Disease relevance of N-Ethyl-N-hydroxyethylnitrosamine

• Histopathological and biochemical analyses of transplantable renal adenocarcinoma in rats induced by N-ethyl-N-hydroxyethylnitrosamine [1].
• For the analysis of different stages in carcinogenesis, Cx32 was assayed in N-ethyl-N-hydroxyethylnitrosamine-induced enzyme altered foci (EAF), hyperplastic nodules (HN), hepatocellular carcinomas (HCC), pulmonary metastatic HCC and transplanted HCC in relation to their degree of altered enzyme expression [2].
• Specific genomic alterations in rat renal cell carcinomas induced by N-ethyl-N-hydroxyethylnitrosamine [3].

High impact information on N-Ethyl-N-hydroxyethylnitrosamine

• The promotion study was conducted with 305 male and 305 female F344 rats fed 170 ppm N-ethyl-N-hydroxyethylnitrosamine in the drinking water for 2 weeks and then inhalation exposed to 0, 10, 70, or 300 ppm UG or 50 ppm TMP for 24 or 59 to 61 weeks [4].
• These latter three compounds have been shown to inhibit hepatocarcinogenesis after initial treatment with N-ethyl-N-hydroxyethylnitrosamine (EHEN) and a significant decrease in the number of enzyme-altered foci and nodules positive for GST-P, GST-A, G6PD and gamma-GT and negative for P-450 PB3a, P-450 MC2 was associated with their administration [5].
• Immunohistochemically demonstrated altered expression of cytochrome P-450 molecular forms and epoxide hydrolase in N-ethyl-N-hydroxyethylnitrosamine-induced rat kidney and liver lesions [6].
• MATERIALS AND METHODS: Chemically [N-ethyl-N-hydroxyethylnitrosamine (EHEN)]-induced non-Eker rat RC lines (designated as BP13 and BP36B) were subjected to PCR-single strand conformation polymorphism (PCR-SSCP) analysis using specific primers covering entire exons of Tsc2 gene (41 coding exons and one non-coding exon) [7].
• Male F344 rats were first treated with diethylnitrosamine (200 mg/kg, i.p.) and then, starting two weeks later, with N-ethyl-N-hydroxyethylnitrosamine (EHEN) for 6 weeks at a dose of 0.01% in drinking water [8].

Biological context of N-Ethyl-N-hydroxyethylnitrosamine

• Absence of ras family point mutations at codons 12, 13 and 61 in N-ethyl-N-hydroxyethylnitrosamine- or N-nitrosomorpholine-induced renal cell tumors in rats [9].
• Preneoplastic and neoplastic liver cell lesions, induced by EHEN (N-ethyl-N-hydroxyethylnitrosamine) in rats, were investigated to establish the numbers of simultaneously expressed altered enzyme phenotypes within the lesion cells [10].

Anatomical context of N-Ethyl-N-hydroxyethylnitrosamine

• Establishment and characterization of three new rat renal cell carcinoma cell lines from N-ethyl-N-hydroxyethylnitrosamine-induced basophilic cell tumors [11].

Associations of N-Ethyl-N-hydroxyethylnitrosamine with other chemical compounds

• The effects of potassium dibasic phosphate (PDP), potassium aluminum sulfate (PAS) and copper sulfate (CS) on early-stage renal carcinogenesis were investigated in unilaterally nephrectomized male Wistar rats after N-ethyl-N-hydroxyethylnitrosamine (EHEN) administration [12].
• The present study was conducted to clarify the effects of N-ethyl-N-hydroxyethylnitrosamine (EHEN) and uracil in combination on renal carcinogenesis in female F344 rats [13].
• The present paper reports the effect of polyphenon-60 (60% pure catechin) on the development of renal cell neoplasms in Wistar rats pretreated with N-ethyl-N-hydroxyethylnitrosamine (EHEN): 0.1% polyphenon-60 in block diet was given over a period of 30 weeks while EHEN was given in drinking water for 2 weeks [14].
• The effect of methimazole on N-ethyl-N-hydroxyethylnitrosamine (EHEN)-induced renal lesions was investigated in a medium-term initiation/promotion bioassay in male Wistar rats [15].
• In an in-vitro test system (Namalva cells), neither NDELA nor N-nitrosoethyl-2-hydroxyethylamine was genotoxic, whereas the corresponding metabolites from alcohol dehydrogenase-mediated oxidation, N-nitroso-2-hydroxymorpholine and N-nitrosoethylethanalamine, induced single-strand breaks even at low doses [16].

Gene context of N-Ethyl-N-hydroxyethylnitrosamine

• We previously reported that Tsc2 mutations were detected in chemically (N-ethyl-N-hydroxyethylnitrosamine (EHEN) and diethylnitrosamine)-induced non-Eker rat RCs, suggesting an involvement of Tsc2 alteration in rat RC development [17].
• N-ethyl-N-hydroxyethylnitrosamine (EHEN)-induced renal and hepatocarcinogenesis in the tumor suppressor Tsc2 transgenic rat [17].

Analytical, diagnostic and therapeutic context of N-Ethyl-N-hydroxyethylnitrosamine

• Sequential observations on the appearance of neoplastic lesions in the liver and kidney after treatment with N-ethyl-N-hydroxyethylnitrosamine followed by partial hepatectomy and unilateral nephrectomy [18].
• Possible application to medium-term organ bioassays for renal carcinogenesis modifiers in rats treated with N-ethyl-N-hydroxyethylnitrosamine and unilateral nephrectomy [19].

References